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The role of vitamins in the prevention and treatment of thyroid disorders

August 2011
Endokrynologia Polska 62(4):340-4

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PubMed

Authors:

Krzysztof Sworczak

Medical University of Gdansk

Piotr Wiśniewski

Medical University of Gdansk

Although vitamin deficiencies are uncommon in Poland or other developed countries, many patients take vitamin supplements. Despite the widespread availability of vitamins and the universal belief that vitamins offer health benefits, few publications have addressed their role in the prevention and treatment of thyroid diseases. There is some evidence to suggest that the administration of vitamins with anti-oxidant properties in patients with hyperthyroidism can decrease the severity of clinical symptoms, and that vitamin D supplementation can have a beneficial effect on the bone system for these patients. It has also been suggested that patients with autoimmune thyroid diseases should be periodically screened for vitamin B12 deficiency. There has been no data to support vitamin supplementation in the primary or secondary prevention of thyroid malignancies.

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340

PRACE POGLĄDOWE/REVIEWS

Endokrynologia Polska/Polish Journal of Endocrinology

Tom/Volume 62; Numer/Number 4/2011

ISSN 0423–104X

The role of vitamins in the prevention and treatment

of thyroid disorders

Rola witamin w zapobieganiu i leczeniu chorób tarczycy

Krzysztof Sworczak, Piotr Wiśniewski

Department of Endocrinology and Internal Diseases, University Clinical Center, Medical University of Gdańsk

Abstract

Although vitamin deficiencies are uncommon in Poland or other developed countries, many patients take vitamin supplements. Despite

the widespread availability of vitamins and the universal belief that vitamins offer health benefits, few publications have addressed their

role in the prevention and treatment of thyroid diseases. There is some evidence to suggest that the administration of vitamins with

anti-oxidant properties in patients with hyperthyroidism can decrease the severity of clinical symptoms, and that vitamin D supplementa-

tion can have a beneficial effect on the bone system for these patients. It has also been suggested that patients with autoimmune thyroid

diseases should be periodically screened for vitamin B12 deficiency. There has been no data to support vitamin supplementation in the

primary or secondary prevention of thyroid malignancies. (Pol J Endocrinol 2011; 62 (4): 340–344)

Key words: hyperthyroidism, thyroid neoplasms, autoimmune thyroid disorder, vitamins

Streszczenie

Chociaż niedobory witamin w Polsce i krajach rozwiniętych zdarzają się rzadko, bardzo duża grupa pacjentów spożywa suplementy

witaminowe. Pomimo powszechnego przekonania o korzystnym wpływie na stan zdrowia oraz szerokiej dostępności niewiele jest publi-

kacji określających ich rolę w zapobieganiu i leczeniu chorób tarczycy. Dane z piśmiennictwa sugerują, że u pacjentów z nadczynnością

tarczycy witaminy o działaniu antyoksydacyjnym mogą zmniejszać nasilenie objawów klinicznych, zaś stosowanie witaminy D może

korzystnie wpływać na stan kośćca w tej grupie chorych. Sugeruje się także, aby pacjentów z autoimmunologiczną chorobą tarczycy

okresowo badać w kierunku niedoboru witaminy B12. Nie ma danych uzasadniających suplementację witamin w prewencji pierwotnej

czy wtórnej nowotworów tarczycy. (Endokrynol Pol 2011; 62 (4): 340–344)

Słowa kluczowe: nadczynność tarczycy, nowotwory tarczycy, autoimmunologiczna choroba tarczycy, witaminy

Krzysztof Sworczak, Department of Endocrinology and Internal Diseases, University Clinical Center, Medical University of Gdańsk,

ul. Dębinki 7, 80–952 Gdańsk, Poland, tel: +48 (58) 349 28 40, fax: +48 (58) 349 28 41, e-mail: ksworczak@gumed.edu.pl



Introduction

Although primary vitamin deficiencies are infre-

quently diagnosed nowadays, sales figures for vita-

min supplements in Poland are high, and continue

to rise. According to “The healthcare and pharmacy

market in Poland 2009. Anticipated development

for the years 2009–2011”, Poland’s pharmacy market

volume in terms of retail prices exceeds 24 billion

zloty, 34% of which is generated by over-the-counter

medications [1]. It is universally accepted that the

use of vitamin supplements prevents many diseases

(e.g. infections or malignancies), increases vitality,

improves mood and enhances treatment of many

disorders. Despite this belief, and the widespread

availability of vitamins, their health impact and role

in the prevention and treatment of diseases remain

insufficiently understood.

Aim of the study

We aimed to review the current state of knowledge on

the possible role of vitamins in patients with thyroid

disorders. This undertaking has proven exceedingly

difficult, as few publications have addressed this issue

in the Polish or the international scientific literature,

and only a few of those that have done so meet current

standards of quality and reliability.

Material and methods

To identify suitable literature, an electronic search

was performed using PubMed. We used the search

string “(*vitamin*[Title] OR antioxidant*[Title]) AND

(*thyroid*[Title] OR goiter*[Title])”. PubMed identified

117 articles written in English or Polish published up to

2010. Titles and abstracts were screened, and 36 publica-

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Endokrynologia Polska/Polish Journal of Endocrinology 2011; 62 (4)

PRACE POGLĄDOWE

tions that were consistent with the study’s objectives

were selected for a full-text reading.

Vitamins with antioxidant properties

(A, C and E)

Cell homeostasis is maintained in part with the help

of the oxidoreductive system which limits the dam-

age caused by the so-called reactive oxygen species

— by-products of the normal metabolism of oxygen.

Its depletion leads to oxidative stress which results in

structural and functional damage. Oxidative stress is

responsible for ageing and plays a role in the develop-

ment of atheromatosis, cancer and Alzheimer’s disease.

Both hyper- and hypothyroidism have been proven

to promote cellular oxidative stress by influencing the

intensity of oxygen reactions. Hyper- and hypothy-

roidism have both been shown to affect concentrations

of the vitamins involved in scavenging of free radicals

(usually decreasing their concentrations, although

study results differ) i.e. vitamins A, C and E. The con-

centrations of those vitamins return to normal after the

achievement of euthyreosis [2–8].

Is supplementation of these vitamins or other anti-

oxidants therefore indicated in patients with thyroid

disorders? That the answer is ‘yes’ has been suggested

by the results of animal studies where administration of

vitamin E in individuals with hyper- or hypothyroidism

reduced oxidative stress, decreased sensitivity to thyroid

hormones, and prevented peroxidation of circulating

LDL lipoproteins [9–11].

In a group of patients with hyperthyroidism due to

Graves’ disease, treated solely with a combination of

antioxidants (vitamin C, vitamin E, beta-carotene, sele-

nium, zinc, copper), clinical symptoms were reduced to

a similar extent as in patients treated with thyreostatic

medications. Moreover, in patients treated with antioxi-

dants, the symptoms of hyperthyroidism subsided more

rapidly, paralleled by decreased markers of oxidative

stress. Given that normalization of thyroid hormone

levels was not observed in this group, the authors sug-

gested that the clinical symptoms of hyperthyroidism

may reflect free radical toxicity and oxidative stress [12].

The beneficial effects of antioxidant supplementation

(with a preparation similar to that used by Guerra)

were also seen in a different study. Patients receiving

antioxidants concomitantly with thyreostatic medica-

tions achieved euthyreosis more rapidly compared to

patients treated with thyreostatics alone [13]. It seems

therefore that supplementation of vitamins C and E, and

possibly other antioxidants, may have beneficial effects

in patients with hyperthyroidism. This issue requires

further study and definitive resolution, especially in

view of other reports suggesting that supplementation

of vitamins A and E may be associated with increased

patient mortality [14].

Conversely, it appears that using antioxidants

in the prevention of thyroid cancer is not justified.

Although results of a retrospective analysis showed

decreased incidence of thyroid cancer in patients tak-

ing beta-carotene, vitamin E or vitamin C [15], recent

meta-analyses and systematic reviews of prospective

studies unequivocally deny anti-neoplastic effects of

antioxidant vitamins [16, 17].

Vitamin A

The metabolism of vitamin A seems fairly closely con-

nected to the activity of the hypothalamic-pituitary-thy-

roid axis. Animal studies show that vitamin A deficiency

is associated with decreased thyroid iodine uptake,

limited synthesis and secretion of hormones, as well

as thyroid enlargement. The total serum triiodothyro-

nine and thyroxine concentrations increase (common

transport proteins e.g. transthyretin bind both thyroid

hormones and the retinol-binding protein, the synthe-

sis of which decreases in vitamin A deficiency). The

rate of hepatic conversion of thyroxine to triiodothy-

ronine is also decreased. Normally, the secretion of

thyroid-stimulating hormone (TSH) is regulated by the

thyroid-hormone-activated receptor and the retinoid X

receptor. The latter, after binding the ligand (vitamin A)

binds with its promoter region of DNA encoding the

beta-subunit of TSH, limiting its expression. Vitamin

A deficiency is thus associated with increased TSH

secretion [18].

This issue has not been as well studied in hu-

mans. Studies conducted in areas of endemic iodine

deficiency have shown that children with goiter and

concomitant vitamin A deficiency were at less risk of

developing hypothyroidism. They also had higher

levels of TSH and thyroxine compared to children

without vitamin A deficiency. A strong correlation

was found between goiter size and severity of vitamin

A deficiency [19]. Monotherapy with vitamin A led to

a decrease in TSH concentrations and reduction in goiter

size, with unchanged serum concentrations of thyroid

hormones [20].

Vitamin B6

Vitamin B6 is a co-enzyme participating in more

than 100 enzymatic reactions in the human body.

Clinically, vitamin B6 is essential for the production

of neurotransmitters, myelin sheaths, hemoglobin,

myoglobin, and the metabolism of homocysteine. Its

deficiency leads to dysfunction of the central nervous

system (manifesting as irritability, mood disturbance,

342

Vitamins and thyroid disorders Krzysztof Sworczak, Piotr Wiśniewski

PRACE POGLĄDOWE

impaired consciousness and seizures), peripheral ner-

vous system (polyneuropathy), as well as anemia and

hyperhomocysteinemia.

There are numerous publications in the medical

literature regarding the role of vitamin B6 in the patho-

genesis and treatment of neurologic, psychiatric and

hematologic diseases, but few on the subject of vitamin

B6 in the context of thyroid dysfunction.

The activity of the hypothalamic-pituitary-thyroid

axis in the setting of vitamin B6 deficiency has been

studied in rats. Well-conducted experiments have

shown that vitamin B6 deficiency leads to hypothy-

roidism resulting from decreased TRH synthesis in the

hypothalamus. The reversal of vitamin B6 deficiency

has led to normalization of thyroid hormone levels

[21]. Over-supplementation of vitamin B6 in human and

animal studies has led to decreased concentrations of

the thyroid-stimulating hormone [22, 23].

No studies have looked at whether hyperthyroidism

or hypothyroidism may lead to vitamin B6 deficiency.

Similarly, there have been no studies on the usefulness

of vitamin B6 supplements in patients treated with

antithyroid agents. According to some physicians,

such treatment may prevent leucopoenia, a fairly com-

mon adverse effect of antithyroid agents. We have not

found a single publication addressing the efficacy of

this measure.

Conversely, there are reports of possible adverse ef-

fects of higher than physiologic doses of vitamin B6. The

daily requirement for vitamin B6 is 2 mg, a level more

than sufficiently provided by the typical diet. Doses not

exceeding 200 mg per day (equivalent to two vitamin

B6 tablets twice daily) are considered safe, whereas

many cases of sensory neuropathy associated with the

administration of larger doses have been reported [24].

Vitamin D

Discoveries made during the last few years have greatly

increased our understanding of the role of vitamin D.

Its influence is not limited to organs involved in calcium

homeostasis (such as the gut, bones, kidneys and par-

athyroid glands). Vitamin D receptors have been found

in more than 35 tissues and it has been demonstrated

to participate in immune processes, insulin secretion,

the regulation of the cardiovascular system and the

development of the central nervous system [25]. Data

on the metabolism of vitamin D in hyperthyroidism

is not consistent. Differences result from factors in-

cluding patient selection, dietary vitamin D intake,

sunlight exposure and seasonal variability of vitamin

D concentration. Both normal [26–28] and decreased

[29–31] concentrations of 25-OH-cholecalciferol have

been found in hyperthyroid patients before treatment.

A study from Japan including 200 euthyrotic patients

with Graves’ disease found vitamin D deficiency in 40%

of women and around 20% of men [32]

It has been demonstrated that hyperthyroidism

leads to reversible loss of bone mass and temporarily

increases the risk of femoral neck fracture [33]. This risk

returns to baseline after approximately a year, whereas

bone mineral density does not return to baseline until

one to four years after treatment of hyperthyroidism

is started [33].

In view of the above, the usefulness of vitamin

D3 supplementation in patients treated for hyperthy-

roidism should be considered, as its possible deficiency

could negatively influence bone healing.

Vitamin B12

Vitamin B12 deficiency may result in a number of neu-

rologic, psychiatric, hematologic, gastrointestinal and

metabolic disturbances (Table I). The commonest etiol-

ogy of decreased absorption of vitamin B12 is atrophic

gastritis which also increases the risk of developing

gastric cancer, hyperplasia of enterochromaffin-like cells

and gastric carcinoid. There is compelling evidence for

the increased prevalence of vitamin B12 deficiency in the

population of patients with thyroid disease.

Centanni et al. examined 62 patients with autoim-

mune thyroid disease (AITD). Patients with increased

serum gastrin underwent endoscopic, pathologic and

immunologic testing. Atrophic gastritis was confirmed

in 22 cases (35%) [34]. Ness-Abramof et al. found de-

creased concentrations of vitamin B12 in 32 out of 115

(28%) patients with AITD. The authors recommended

routine measurements of vitamin B12 every 3-5 years

in these patients. In those with decreased vitamin B12

concentrations, further management should depend

on the level of gastrin, as the presence of hypergas-

trinemia is highly suggestive of concomitant atrophic

Table I. Clinical sequelae of vitamin B12 deficiency

Tabela I. Kliniczne następstwa niedoboru witaminy B12

Neurological symptoms Non-neurological symptoms

Peripheral neuropathy Glossitis

Subacute combined Gastrointestinal disturbances

degeneration of spinal cord Weight loss

Focal demyelination Anemia

of white matter in the brain

Optic nerve Impaired fertility

inflammation/atrophy

Psychiatric symptoms Hyperhomocysteinemia

(depression, cognitive deficit,

psychosis)

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Endokrynologia Polska/Polish Journal of Endocrinology 2011; 62 (4)

PRACE POGLĄDOWE

gastritis [35]. The suggested management algorithm is

summarized in Figure 1.

Orzechowska-Pawilojc et al. found that both the

hypothyroid [36] and hyperthyroid [37] state in women

is associated with lower concentration of vitamin B12

when compared to a healthy control group. However,

the authors did not report the higher prevalence of

vitamin B12 deficiency in the study groups [36, 37].

Summary

It seems that the only indisputable conclusion of the

current literature regarding the role of vitamins in pa-

tients with thyroid disorders is that this issue requires

further study. With that in mind, a physician caring

for patients with thyroid disorders should realize that

supplementation of antioxidant vitamins probably does

not prevent thyroid malignancies, but can decrease

symptoms in patients with hyperthyroidism. It is also

possible that supplementation of vitamin D in these

patients accelerates bone healing. There is no scientific

data justifying supplementation of vitamin B6 in these

patients. Atrophic gastritis often coexists with autoim-

mune thyroid disease and periodic evaluation of vita-

min B12 levels seems justified in this patient population.

When counselling patients about the use of vitamin

supplements, it should be remembered that several

studies have demonstrated adverse consequences of

their action.

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Jul 2022

Context: Calorie restriction reduces circulating triiodothyronine (T3) – the most active thyroid hormone – inducing hypothyroidism, constipation, and reduced appetite that inhibit eating, acting to sustain and sometimes precipitate eating disorders. Thyroid-hormone treatment can be effective but is rarely employed. Case description: A 12-year-old girl experienced chronic nausea and constipation after antibiotics for strep throat, resulting in restricted eating. Energy decreased for 2 months as anxiety and depression increased, culminating in withdrawal and school refusal. Blood tests were normal except for below-range free T3. She began a trial of incremental, 1-μg dose increases of T3 every 3 days using sustained-release capsules added to her established triiodothyronine–levothyroxine (T3–T4) protocol for hypothyroidism. Her energy and mood began improving after 10 days and depression resolved after 7 weeks. An 18-day stay in a hospital eating-disorders unit helped her regain some weight and strength. To address nausea and anxiety, the extended medical team then tried two antidepressants and cyproheptadine – each caused increased nausea and reduced eating – and a 5-day prednisone burst for possible neuroinflammation; all were ineffective and discontinued. After 14 weeks without improvement, we resumed adjusting thyroid-hormone dose. Anxiety, energy, food intake, and weight improved for 5 months. She began attending a new school, developed new friendships, and started menses. The major illness lasted 21 months. T3 intake increased from 5 to 27 μg, T4 from 50 to 110 μg, weight from 36.4 to 52.7 kg, and height from 1.63 to 1.71 m. Conclusions: Thyroid hormones should be studied further as fundamentally effective treatment for eating disorders. Keywords: Eating disorder; Low-triiodothyronine syndrome; Hypothyroidism

The protective effect of hesperidin on the liver of hypothyroid rats mediated by nuclear factor erythroid 2-related factor 2-dependent activation of heme oxygenase 1

Article

Full-text available

Jun 2022
J MOL HISTOL

Hypothyroidism (HPO) has been linked to a higher incidence of hepatic lesions. Hesperidin (HSP) is an antioxidant, anti-adipogenic, anti-inflammatory, anti-hyperlipidemic, and anti-apoptotic agent. Therefore, the study aimed to assess the impact of carbimazole (CBZ)-induced HPO on adult albino rats’ liver and explore the possible ameliorating effect of Eltroxin (ELT) and HSP. HPO was induced by CBZ (20 mg/kg/day). Rats were allocated into group I: normal control; group II: received CBZ (20 mg/kg/day) only; group III: received CBZ and HSP (200 mg/kg/day); and group IV: received CBZ and ELT (0.045 mg/kg/day). HSP and ELT attenuated dyslipidemia associated with HPO. HSP and ELT also significantly decreased elevated malondialdehyde and increased reduced glutathione levels and superoxide dismutase and catalase activities. Also, they markedly inhibited the expression of nuclear factor kappa B, inducible nitric oxide synthase, interleukin (IL)-1β, tumor necrosis factor-alpha, and alpha-smooth muscle actin. On the other hand, HSP successfully elevated nuclear factor erythroid 2-related factor 2, heme oxygenase 1, IL-37, proliferating cell nuclear antigen, and B-cell lymphoma 2 levels. Moreover, HSP decreased the activity of liver transaminases and increased total protein and albumin levels. HSP showed a protective effect on liver tissues of CBZ-treated rats. Our findings confirmed that HSP is an effective antioxidant that prevents and protects the liver from damage by CBZ. Therefore, HSP is a promising candidate for future use to minimize and alleviate HPO risks. Graphical abstract

Measurement of oxidative stress and total antioxidant capacity in hyperthyroid patients following treatment with carbimazole and antioxidant

Article

Full-text available

Dec 2021

Hyperthyroidism is a common endocrine disorder in which the thyroid produces too many hormones, resulting in the metabolism speed up. The present study was designed to measure oxidative stress and total antioxidant capacity in hyperthyroid patients following treatment with carbimazole and antioxidants supplements. This randomized clinical trial study was conducted to compare Malondialdehyde (MDA) and total antioxidant capacity (TAC) among 25 newly diagnosed hyperthyroid patients (Group A), 25 hyperthyroid patients treated with carbimazole (Group B) and 25 hyperthyroid patients treated with carbimazole and antioxidants supplement (Group C) of both sexes. In this study, the mean serum malondialdehyde (MDA) of the three groups were 4.60±1.08 μmol/L (Group A), 2.79±0.58 μmol/L(Group B), and 1.57±0.29 μmol/L (Group C). We found the mean MDA level was significantly higher in Group A than Group B and Group C. This study found the MDA level was significantly higher in hyperthyroid patients treated with carbimazole alone (Group B, 2.79±0.58 umol/L) than hyperthyroid patients treated with carbimazole and antioxidant combined (Group C, 1.57±0.29 umol/L) among the study groups (p<0.001). The results showed that the mean serum TAC was significantly lower in newly diagnosed hyperthyroid (Group A, 527.8±78.44 umol/L] patients compared to carbimazole treated alone (Group B,951.80±99.67 umol/L) and combination with the antithyroid drug (carbimazole) and antioxidant treated (Group C, 1113.56±121.69 umol/L). There was more improvement found in the treatment combined with the antithyroid drug (carbimazole) and antioxidant (Group C). Conventional treatment of hyperthyroid patients significantly reduced oxidative stress and elevated serum TAC but not up to normal level. Therefore, the supplementation of antioxidants could be utilized to improve thyroid function in hyperthyroid patients by boosting antioxidants and restoring oxidant-antioxidant balance. However, further studies are required to determine the optimal dosage, route of administration, and timing of antioxidant therapy needed before this supplementation could be officially recommended as adjuvant therapy.

Problematic rise of vitamin B6 supplementation overuse and potential risk to bariatric surgery patients

Article

May 2022

Objectives: Due to the increased prevalence of obesity in the world, bariatric surgeries are on the rise and necessitate life-long surveillance for deficiencies; hence the recommended vitamin supplementation in these patients. However, inadequate multivitamin supplementation may induce vitamin B6 overload. Methods: We reviewed all vitamin B6 dosages at the university hospitals of Poitiers, Tours, Bordeaux, and Limoges for the past 5 to 8 years. Analyses were performed by high-performance liquid chromatography, coupled with a fluorescence detector on whole blood samples. Results: During the study period, there was an increase in the number of vitamin B6 dosages. Deficiencies were detected early in Poitiers and Limoges, but were negligible by 2020. However, during the same time period, the number of overdoses increased, reaching close to 40% of dosages at all centers. Conclusions: Pyridoxin overload is not possible through food-derived pyridoxin; hence, combined with the fact that most vitamin supplements contain vitamin B6, inadequate vitamin supplementation is likely the cause of the observed increase in overdoses. High doses of vitamin B6 can induce polyneuropathy, particularly targeting motor neurons; thus, the increase of overdoses is worrying. In light of the possible risks and the ease with which these could be averted (better formulation of supplements), the precaution principle requires a definition of clear guidelines for vitamin supplementation, especially in patients undergoing bariatric surgery.

Wybrane Choroby Cywilizacyjne XXI Wieku - Wybrane wymiary osobowości a strategie radzenia ze stresem u osób zdrowych i chorych na schizofrenie

Chapter

Full-text available

Jan 2017

For years, considerations of clinical psychologists have focused on related discussions with health and illness, asking questions about the limits of identity, norms and quality of life. Schizophrenia is still a big mystery to today's medicine - the different types of it the diseases do not have clearly defined causes, so it is still not possible to develop it fully effective and universal therapy. The notion that each person is a separate entity with a "I" is fundamental to undertake theoretical considerations in order to understand the various aspects of learning oneself, perceptions, development of motivation, emotions combine to form the full picture of the individual personality and create the opportunity to live life on your own, individual level functioning. Personality makes it possible to call oneself people and shows that no two units are alike in the world [1]. The choice of topic is justified by the search for answers to bothering questions: whether selected personality dimensions such as neuroticism and extraversion correlate with coping strategies? Is there a relationship between the strategies coping with stress among healthy people and patients with schizophrenia? Answers have been shown in the light of the historical trait of clinical psychology so far conducted research and analysis of the results of own research giving the possibility of deepening the topic at hand. This article is empirical in nature. Its purpose is to understand the relationship between selected personality dimensions and styles of coping with stress. Theoretical part

Developmental effects of sesamolin on zebrafish (Danio rerio) embryos

Article

Feb 2022
COMP BIOCHEM PHYS C

Sesamolin is one of the major active compounds found in sesame seeds (Sesamum indicum L.) that are commonly and increasingly used as an ingredient in cuisines and various food products. The compound has been reported to have several pharmaceutical activities such as antioxidant, antimicrobial, neuroprotective, and anticancer. However, the toxicological profile of sesamolin does not currently include developmental toxicity. In this study, we assessed sesamolin toxicity to embryonic development of zebrafish by exposure for 72 h at concentrations ranging from 10 to 50 μM. The evaluation revealed that sesamolin did not affect survival and hatching rates. However, it did induce embryo malformations and reduced embryonic heart rates in a dose-dependent manner. By qRT-PCR analysis, it downregulated the expression of oxidative stress-related genes, including superoxide dismutase 1 (sod1), catalase (cat), and glutathione S-transferase pi 2 (gstp2). Alkaline phosphatase staining of embryos revealed that sesamolin inhibited the development of subintestinal vessels, and hemoglobin staining revealed a negative impact on embryonic erythropoiesis. These findings showed that sesamolin affected genes related to angiogenesis and erythropoiesis. The risks of sesamolin to embryonic development found in this study may imply similar effects in humans and other mammals.

Effects of Vitamin E and Vitamin C supplementation on plasma lipid peroxidation and on Oxidation of apolipoprotein B-Containing lipoproteins in experimental hyperthyroidism

Article

Full-text available

Jul 1999

Increasing numbers of experimental and epidemiological studies suggest the involvement of free radicals in the pathogenesis of various disease entities. Similarly, oxidative processes have been implicated as playing roles in the genesis of hyperthyroidism-induced damage. In this study, we investigated the effects of vitamin E and vitamin C on plasma lipid peroxidation and the susceptibility of apolipoprotein B (apo B)-containing lipoproteins to oxidation in experimental hyperthyroidism. The study animals were initially divided into a control group (Group C) and a hyperthyroid group. The latter was further re-grouped later according to their vitamin supplementation status: Hyperthyroid group without vitamin supplementation (Group H), hyperthyroid group with vitamin E supplementation (Group H+E) and hyperthyroid group with vitamin C supplementation (Group H+C). Malondialdehyde (MDA) level was measured as an indicator of plasma lipid peroxidation. The apo B-containing lipoproteins were separated by precipitation and incubated with copper sulphate. The MDA levels of this non-HDL fraction were measured prior to and after 1, 2 and 3 hours of incubation. Plasma MDA levels showed no significant differences among groups. Whereas MDA levels measured in non-HDL fraction were significantly higher in Group H than Group C. Group H+E and Group H+C had significantly lower MDA levels than Group H in all these measurements. This finding strongly indicates an increased susceptibility of apo B-containing lipoproteins to oxidation in hyperthyroidism, and that vitamin E as well as vitamin C supplementation protect these lipoproteins from copper-induced oxidation.

Ceruloplasmin and vitamin E levels in toxic multinodular goiter

Article

Full-text available

Feb 1996
NUTR RES

The effect of the enhanced metabolic rate over antioxidant status was investigated in hyperthyroid individuals. Serum total T3 and T4 levels were measured by radioimmunoassay in 45 patients and 25 controls. The serum vitamin E was assayed fluorometrically in the hexane extract of serum. Serum ceruloplasmin activity was measured spectrophotometrically. Statistical significance was asessed by correlation regression analysis and paired t-test. The serum vitamin E levels decreased significantly as the levels of the thyroid hormones increased. For ceruloplasmin the opposite changes were observed: mean serum ceruloplasmin of hyperthyroid patients was greater than that of control group. Although the changes in vitamin E and ceruloplasmin concentrations did correlate with the levels of thyroid hormones in hyperthyroid patients, we observed no associations between these parameters in the euthyroid state. As these two parameters are the measure of oxidation potential, it may be suggested that raised free radical activity in hyperthyroidism cause the increased oxidative stress and increased general radical scavenging. The present data may indicate a direct effect of thyroid hormones on vitamin E and ceruloplasmin metabolism.

Homocysteine, Folate and Cobalamin Levels in Hypothyroid Women before and after Treatment

Article

Full-text available

Jun 2007

Hyperhomocysteinaemia is an independent risk factor for premature atherosclerotic vascular disease and venous thrombosis. Hypothyroidism is associated with mild hyperhomocysteinaemia. The aim of the present study was to assess plasma total homocysteine (tHcy) and its determinants (folate, cobalamin) in hyperthyroid patients before and after treatment. Thirty hyperthyroid and thirty healthy premenopausal women were studied. The hyperthyroid patients were investigated in the untreated state and again after restoration of euthyroidism. The levels of homocysteine, folate, cobalamin, and thyroid stimulating hormone (TSH), free thyroxine (fT(4)), free triiodothyronine (fT(3)), and renal function were measured before and after treatment. In hyperthyroidism, tHcy was lower than in the control group. The serum level of folate was higher and serum cobalamin was lower in the hyperthyroid state. Following antithyroid drug therapy, tHcy significantly increased and folate decreased. The level of cobalamin remained unchanged. Univariate analysis in the hyperthyroid group indicated that tHcy significantly negatively correlated only with fT(3). Lower homocysteine levels in hyperthyroid state can be explained by the influence of thyroid hormone. High level of folate is only partially responsible for these changes.

From Vitamin D to hormone D: Fundamentals of the Vitamin D endocrine system essential for good health

Article

Full-text available

Aug 2008
AM J CLIN NUTR

Anthony W Norman

New knowledge of the biological and clinical importance of the steroid hormone 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)] and its receptor, the vitamin D receptor (VDR), has resulted in significant contributions to good bone health. However, worldwide reports have highlighted a variety of vitamin D insufficiency and deficiency diseases. Despite many publications and scientific meetings reporting advances in vitamin D science, a disturbing realization is growing that the newer scientific and clinical knowledge is not being translated into better human health. Over the past several decades, the biological sphere of influence of vitamin D(3), as defined by the tissue distribution of the VDR, has broadened at least 9-fold from the target organs required for calcium homeostasis (intestine, bone, kidney, and parathyroid). Now, research has shown that the pluripotent steroid hormone 1alpha,25(OH)(2)D(3) initiates the physiologic responses of >/=36 cell types that possess the VDR. In addition to the kidney's endocrine production of circulating 1alpha,25(OH)(2)D(3,) researchers have found a paracrine production of this steroid hormone in >/=10 extrarenal organs. This article identifies the fundamentals of the vitamin D endocrine system, including its potential for contributions to good health in 5 physiologic arenas in which investigators have clearly documented new biological actions of 1alpha,25(OH)(2)D(3) through the VDR. As a consequence, the nutritional guidelines for vitamin D(3) intake (defined by serum hydroxyvitamin D(3) concentrations) should be reevaluated, taking into account the contributions to good health that all 36 VDR target organs can provide.

Efficacy of antioxidant supplementation in reducing primary cancer incidence and mortality: Systematic review and meta-analysis

Article

Jan 2008

OBJECTIVE: To estimate the association between antioxidant use and primary cancer incidence and mortality and to evaluate these effects across specific antioxidant compounds, target organs, and participant subgroups. METHODS: Multiple electronic databases (MEDLINE, Cochrane Controlled Clinical Trials Register, EMBASE, Science Citation Index) were searched from their dates of inception until August 2005 to identify eligible randomized clinical trials. Random effects meta-analyses estimated pooled relative risks (RRs) and 95% confidence intervals (CIs) that described the effect of antioxidants vs placebo on cancer incidence and cancer mortality. RESULTS: Twelve eligible trials, 9 of high methodological quality, were identified (total subject population, 104,196). Antioxidant supplementation did not significantly reduce total cancer incidence (IRR, 0.99; 95% CI, 0.94-1.04) or mortality (RR, 1.03; 95% CI, 0.92-1.15) or any site-specific cancer incidence. Beta carotene supplementation was associated with an increase in the incidence of cancer among smokers (RR, 1.10; 95% CI, 1.03-1.10) and with a trend toward increased cancer mortality (RR, 1.16; 95% CI, 0.98-1.37). Selenium supplementation was associated with reduced cancer incidence in men (RR, 0.77; 95% CI, 0.64-0.92) but not in women (IRR, 1.00; 95% CI, 0.89-1.13, value for interaction, P<.001) and with reduced cancer mortality (RR, 0.78; 95% CI, 0.65-0.94). Vitamin E supplementation had no apparent effect on overall cancer incidence (RR, 0.99; 95% CI, 0.941.04) or cancer mortality (RR, 1.04; 95% CI, 0.97-1.12). CONCLUSION: Beta carotene supplementation appeared to increase cancer incidence and cancer mortality among smokers, whereas vitamin E supplementation had no effect. Selenium supplementation might have anticarcinogenic effects in men and thus requires further research.

Mortality in randomized trials of antioxidant supplements for primary and secondary prevention. Systematic review and meta-analysis

Article

Jan 2007

On page 845 in the first paragraph of the “All Randomized Trials” subsection, the sentence that read “Heterogeneity was not significant (I²=18.6%, P=.10)” should have read “Heterogeneity was significant (I²=18.9%, P=.10).” In the following sentence that begins “Adjusted-rank correlation test (P=.08), but not the regression asymmetry test (P=.26), suggested the bias among trials,” the respective P values should have read “(P=.09)” and “(P=.24).” In the second paragraph of the same subsection, the portion of the sentence that begins on page 845: “Univariate meta-regression analyses revealed significant influences of dose of beta carotene (RR, 1.004; 95% CI, 1.001-1.007; P=.012),” the P value should have been equal to “.014.” In the latter part of the same sentence that falls on page 847, the P value for the dose of selenium that read “P=.002” should have read “P=.001.” In the following part of the sentence, the upper confidence limit that read “1.29” should have read “1.30.” In the third paragraph of the same subsection, on page 847, the P value for the “multivariate meta-regression” for dose of selenium that read “P=.005” should have read “P=.004,” the lower confidence limit for low-bias risk trials that read “1.05” should have read “1.04,” and the P value for the low-bias risk trials in the same sentence that read “P=.005” should have read “P=.006.” In Table 5 on page 853, the RR (95% CI) in the “Beta carotene given singly” row that read “1.06 (1.01-1.11)” should have read “1.05 (1.00-1.11)” and the I² value that read “5.4” should have read “11.8.” In the “Beta carotene given in combination with other antioxidant supplements” row, the I² value that read “55.6” should have read “55.5.” In the “Beta carotene given singly or in combination with other antioxidant supplements” row, the CI range that read “(0.96-1.08)” should have read “(0.95-1.07)” and the I2 value that read “52.2” should have read “52.5.” In the “Beta carotene given singly or in combination with other antioxidant supplements after exclusion of high-bias risk and selenium trials” row, the I² value that read 36.8” should have read “34.4” In the “Vitamin E given singly” row, the number of study participants that read “47 007” should have read “41 341.” In the “Vitamin E given in combination with other antioxidant supplements” row, the RR that read “1.01” should have read “1.00” and the I² value that read “17.2” should have read “16.9.” In the “Vitamin E given singly or in combination with other antioxidant supplements” row, the I²value that read “2.8” should have read “2.4.” In the “Vitamin E given singly or in combination with other antioxidant supplements after exclusion of high-bias risk and selenium trials” row, the list of references should have included reference 87 and excluded 95.

Vitamin Supplements and Cancer Prevention: Where Do Randomized Controlled Trials Stand?

Article

Jan 2009
J NATL CANCER I

Demetrius Albanes

Vitamin D levels in thyrotoxicosis

Article

Mar 1977

Serum-25-hydroxycholecalciferol in hyperthyroidism

Article

May 1977

Suppression of Thyrotropin (TSH) and Prolactin (PRL) Release by Pyridoxine in Chronic Primary Hypothyroidism

Article

Dec 1977

A single iv dose of pyridoxine (V) (300 mg) caused a significant decrease in the concentration of serum thyrotropin (TSH) in 6 patients with primary hypothyroidism. There was no consistent change in serum thyroxine and triiodothyronine concentrations suring the experiment. The serum prolactin (PRL) levels were also suppressed by pyridoxine administration. These findings suggest that pyridoxine inhibits TSH secretion as well PRL by a direct action on the hypothalamus or pituitary gland.

The role of vitamins in the prevention and treatment of thyroid disorders

Abstract

Recommendations

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